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Possible new therapeutic strategy to regulate atopic dermatitis through upregulating filaggrin expression.
Otsuka, Atsushi; Doi, Hiromi; Egawa, Gyohei; Maekawa, Akiko; Fujita, Tomoko; Nakamizo, Satoshi; Nakashima, Chisa; Nakajima, Saeko; Watanabe, Takeshi; Miyachi, Yoshiki; Narumiya, Shuh; Kabashima, Kenji.
Afiliación
  • Otsuka A; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan; Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Doi H; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Egawa G; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Maekawa A; Department of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Fujita T; Department of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Nakamizo S; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Nakashima C; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Nakajima S; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Watanabe T; Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Miyachi Y; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Narumiya S; Department of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Kabashima K; Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. Electronic address: kaba@kuhp.kyoto-u.ac.jp.
J Allergy Clin Immunol ; 133(1): 139-46.e1-10, 2014 Jan.
Article en En | MEDLINE | ID: mdl-24055295
BACKGROUND: Nonsense mutations in filaggrin (FLG) represent a significant genetic factor in the cause of atopic dermatitis (AD). OBJECTIVE: It is of great importance to find drug candidates that upregulate FLG expression and to determine whether increased FLG expression controls the development of AD. METHODS: We screened a library of bioactives by using an FLG reporter assay to find candidates that promoted FLG mRNA expression using a human immortalized keratinocyte cell line (HaCaT). We studied the effect of the compound on keratinocytes using the human skin equivalent model. We examined the effect of the compound on AD-like skin inflammation in NC/Nga mice. RESULTS: JTC801 promoted FLG mRNA and protein expression in both HaCaT and normal human epidermal keratinocytes. Intriguingly, JTC801 promoted the mRNA and protein expression levels of FLG but not the mRNA levels of other makers for keratinocyte differentiation, including loricrin, keratin 10, and transglutaminase 1, in a human skin equivalent model. In addition, oral administration of JTC801 promoted the protein level of Flg and suppressed the development of AD-like skin inflammation in NC/Nga mice. CONCLUSION: This is the first observation that the compound, which increased FLG expression in human and murine keratinocytes, attenuated the development of AD-like skin inflammation in mice. Our findings provide evidence that modulation of FLG expression can be a novel therapeutic target for AD.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Benzamidas / Queratinocitos / Dermatitis Atópica / Aminoquinolinas / Proteínas de Filamentos Intermediarios Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: J Allergy Clin Immunol Año: 2014 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Benzamidas / Queratinocitos / Dermatitis Atópica / Aminoquinolinas / Proteínas de Filamentos Intermediarios Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: J Allergy Clin Immunol Año: 2014 Tipo del documento: Article País de afiliación: Japón Pais de publicación: Estados Unidos